Cardiac Workload Research Articles

Maturation of Cardiac Energy Metabolism During Perinatal Development.

As one of the highest energy consumer organ in mammals, the heart has to be provided with a high amount of energy as soon as its first beats in utero. During the development of this organ, energy is produced within the cardiac muscle cell depending on substrate availability, oxygen pressure and cardiac workload that drastically change at birth. Thus, energy metabolism relying essentially on carbohydrates in fetal heart is very different from the adult one and birth is the trigger of a profound maturation which ensures the transition to a highly oxidative metabolism depending on lipid utilization. To face the substantial increase in cardiac workload resulting from the growth of the organism during the postnatal period, the heart not only develops its capacity for energy production but also undergoes a hypertrophic growth to adapt its contractile capacity to its new function. This leads to a profound cytoarchitectural remodeling of the cardiomyocyte which becomes a highly compartmentalized structure. As a consequence, within the mature cardiac muscle, energy transfer between energy producing and consuming compartments requires organized energy transfer systems that are established in the early postnatal life. This review aims at describing the major rearrangements of energy metabolism during the perinatal development.

Cardiovascular responses to cold and submaximal exercise in patients with coronary artery disease.

Regular year-round exercise is recommended for patients with coronary artery disease (CAD). However, the combined effects of cold and moderate sustained exercise, both known to increase cardiac workload, on cardiovascular responses are not known. We tested the hypothesis that cardiac workload is increased, and evidence of ischemia would be observed during exercise in the cold in patients with CAD. Sixteen men (59.3 ± 7.0 yr, means ± SD) with stable CAD each underwent 4, 30 min exposures in a randomized order: seated rest and moderate-intensity exercise [walking, 60%-70% of max heart rate (HR)] performed at +22°C and -15°C. Systolic brachial blood pressure (SBP), HR, electrocardiogram (ECG), and skin temperatures were recorded throughout the intervention. Rate pressure product (RPP) and ECG parameters were obtained. The combined effects of cold and submaximal exercise were additive for SBP and RPP and synergistic for HR when compared with rest in a neutral environment. RPP (mmHg·beats/min) was 17% higher during exercise in the cold (18,080 ± 3540) compared with neutral (15,490 ± 2,940) conditions ( P = 0.001). Only a few ST depressions were detected during exercise but without an effect of ambient temperature. The corrected QT interval increased while exercising in the cold compared with neutral temperature ( P = 0.023). Recovery of postexercise blood pressure was similar regardless of temperature. Whole body exposure to cold during submaximal exercise results in higher cardiac workload compared with a neutral environment. Despite the higher RPP, no signs of myocardial ischemia or abnormal ECG responses were observed. The results of this study are useful for planning year-round exercise-based rehabilitation programs for stable CAD patients.

Coital Hemoptysis Due to Cardiac AL Amyloidosis

A 48-year-old woman presented with recurrent hemoptysis during intercourse. The computed tomography (CT) pulmonary angiogram demonstrated bilateral patchy ground glass opacities and no pulmonary embolism and a small pulmonary cyst (Figure A, arrow). She was treated with azithromycin, and follow-up chest CT 12 days later demonstrated complete resolution (Figure D). Stress echocardiogram suggested multivessel coronary artery disease (CAD), but coronary angiogram demonstrated only mild CAD. An exercise right-heart catheterization showed exercise-induced pulmonary arterial hypertension and elevated filling pressures. Cardiac magnetic resonance imaging showed delayed subendocardial enhancement, left ventricular hypertrophy, and biatrial enlargement (Supplemental Figure: 3-chamber and 4-chamber views, available online at http://www.mayoclinicproceedings.org). Subsequent right ventricular biopsy at 200× magnification showed a pericellular pattern of amyloid deposition (Figure B, arrow) on Congo red stain with characteristic apple-green birefringence (Figure C, arrow) under polarized light diagnostic of AL (lambda) cardiac amyloidosis. Coital hemoptysis is infrequently described and typically due to cardiac etiology such as heart failure, mitral valve disease, or CAD.1Fuks L. Shitrit D. Amital A. Fox B.D. Kramer M.R. Postcoital hemoptysis: our experience and review of the literature.Respir Med. 2009; 103: 1828-1831Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar Amyloidosis is an uncommon cause of hemoptysis, but more often due to pulmonary parenchymal disease and pulmonary vascular fragility rather than cardiac disease.2Road J.D. Jacques J. Sparling J.R. Diffuse alveolar septal amyloidosis presenting with recurrent hemoptysis and medial dissection of pulmonary arteries.Am Rev Respir Dis. 1985; 132: 1368-1370PubMed Google Scholar We hypothesize that when imposed on a noncompliant, amyloid-infiltrated heart, increased cardiac workload and systemic arterial pressures during intercourse caused a dramatic elevation in left ventricular filling pressures leading to flash pulmonary edema. The cystic pulmonary lesion may indicate pulmonary involvement, with possible increased pulmonary microvascular involvement and a predisposition to hemoptysis. If present, pulmonary microvascular involvement may have predisposed to hemoptysis in the setting of rapidly increased cardiac filling pressures. After a positive serum protein electrophoresis, a bone marrow biopsy revealed multiple myeloma for which the patient underwent autologous stem cell transplant and is doing well. We thank Omar F. AbouEzzeddine, MDCM, MS, and Mandeep Singh, MD, MPH, for their mentorship and assistance in manuscript preparation. Supplemental material can be found online at http://www.mayoclinicproceedings.org. Supplemental material attached to journal articles has not been edited, and the authors take responsibility for the accuracy of all data.

Anxiety-Related Bleeding and Thrombosis.

Anxiety, a normal response to stressful situations, is characterized by increased levels of factor VIII, fibrinogen, and von Willebrand factor, and by enhanced platelet aggregability. One would expect acute anxiety to be a prothrombotic state, but since acute mental stress induces tissue plasminogen activator (tPA) release from endothelial and chromaffin cells, fibrinolysis counteracts procoagulant stimuli. It could be said that procoagulant changes accompanying the fight-or-flight response reduce the risk of bleeding in case of potential injuries, while activation of fibrinolysis counteracts activation of hemostasis to prevent intravascular thrombus formation before injuries occur. Acutely anxious patients are prone to bleeding or thrombosis when the balance between hypercoagulation and hyperfibrinolysis is disturbed. Acute anxiety not only increases the risk of bleeding in hemophilia or von Willebrand disease, but many reports have shown that anxiolytic interventions such as hypnosis are effective in controlling bleeding in hemostatic disorders. The pathogenesis of cardiovascular and thrombotic diseases in highly anxious patients is multifactorial. An important element is α-adrenergic vasoconstriction, which increases viscosity due to leakage of intravascular fluid into the interstitium, and also causes hypertension, favoring plaque rupture. Paradoxical as it may seem, over secretion of tPA may increase cardiovascular risk. This is because tPA degrades the extracellular matrix, causing vascular stiffness that increases cardiac workload, and thus oxygen requirements. Anxious patients with conditions associated with increased plasminogen activator inhibitor-1 levels, such as depression or postprandial hyperinsulinemia, are at high risk of thrombosis. Postprandial hyperinsulinemia may result from consumption of high-carbohydrate foods, considered anxiolytic, combined with a sedentary life, which is common among anxious individuals. Preliminary evidence suggests that high anxiety combined with either depression or a lifestyle that results in hyperinsulinemia has an important role in the pathogenesis of thrombotic events currently classified as unprovoked.

Intracellular Remodeling in a Rodent Model of Cardiac Mechanical Unloading - Influence of Phospholamban on Expression of Cardiac Ion Currents

Unloading of failing hearts by LVADs can improve cardiac function, but also lead to negative alterations in cardiac myocyte physiology, e.g. arrhythmias, associated with increased morbidity and mortality. A reduction in cardiac workload itself induces a remodeling of cellular electrophysiology for example of action potentials and underlying repolarizing ionic currents. Previous work suggests a pivotal role of phospholamban (PLN) for orchestrating the ion channel remodeling during unloading. To test this hypothesis we analyzed ion channel remodeling in unloaded PLN knock-out (PLN -/-) mice hearts.

Hemodynamic Effects of an Intra-aortic Micro-axial Flow Pump in a Swine Model of Ischemic Heart Failure

Heart failure is major cause of global morbidity and mortality and is exacerbated by renal hypo-perfusion leading to worsening congestion. Increasing cardiac ouput, reducing cardiac workload, and increasing renal perfusion are major objectives for heart failure management. We explored the hemodynamic effect of a micro-axial flow pump (Aortix) positioned in the abdominal aorta above the renal arteries in a model of ischemic heart failure.

CRT-600.11 Uncoupling Cardio-renal Hemodynamics in Heart Failure: Effects of an Intra-aortic Micro-axial Flow Pump in a Swine Model of Ischemic Heart Failure

Heart failure complicated by renal hypo-perfusion is a major cause of global morbidity and mortality. Increasing cardiac output, reducing cardiac workload, and increasing renal perfusion are major objectives for heart failure management. We explored the hemodynamic effect of a micro-axial flow pump

Handrail Support Produces a Higher Rate Pressure Product in Apparently Healthy Non-Treadmill Users During Maximal Exercise Testing

Objective: Exercise treadmill testing (ETT) is a well-established procedure for the diagnosis, prognosis and functional assessment of patients with suspected cardiovascular disease. The use of handrail support during ETT is often discouraged as this has been demonstrated to overestimate functional capacity. It is unknown if this increase in functional capacity translates to an increase in cardiac workload. The aim of this study was to investigate if the use of handrail support during maximal ETT produces an increase in cardiac workload when compared to no handrail support. Approach: Fifty-two consenting volunteers performed two maximal ETTs, one with handrail support and the other without, approximately one week apart. Participants were identified as either experienced treadmill users (treadmill use >= once per fortnight) (n = 24) or inexperienced users (n = 28). Cardiac workload was quantified using rate pressure product (RPP) (systolic blood pressure (SBP) x heart rate (HR)) Main results: The average age of participants was 38.4 +/- 11.4 years (44% male). Overall exercise duration was significantly prolonged by 44.4% with handrail support (with support 15:01 +/- 2:54 min; without support 10:24 +/- 2:09 min). Overall HR, SBP and maximum RPP were not significantly different between conditions. For the 28 inexperienced treadmill users maximum RPP was significantly higher during handrail support (7.5% increase) (with support 34 417 +/- 4906; without support 31 821 +/- 4565). Significance: Handrail support overestimates functional capacity, however produces greater maximal RPP in inexperienced treadmill users. If accurate aerobic data is required during ETT, or subjects performing ETT are experienced treadmill users, handrail support should be discouraged. Non-treadmill users or subjects fearful of falling may benefit from handrail support, particularly when maximal cardiac workload is desired.

Effect of Laparoscopic Ovarian Drilling on Anti-Müllerian Hormone Level among Women with Polycystic Ovary Syndrome : A Retrospective Study

Background: Thyroid dysfunction is associated with increased cardiovascular morbidity and mortality. Hyperthyroidism increases the susceptibility of the heart to ischemia reperfusion injury. Moreover, myocardial ischemia can be further worsened by increased cardiac workload and oxygen demand elicited by the excess thyroid hormones. Objectives: Investigating the cardiac dysfunction induced by ischemia-reperfusion (IR) in rats exposed to excess thyroid hormones and role of somatostatin analogue against ischemia/reperfusion injury in hyperthyroid rats. Patients and Methods: This study was performed on 24 adult male albino rats of a local strain weighing 140-200 g, allocated into three equal groups: Group I (Control IR group): Euthyroid control group exposed to ischemia-reperfusion. Hearts of this group were isolated and perfused in a Langendorff apparatus. Isolated hearts were subjected to 15 min of stabilization, 20 min of zero-flow global ischemia and 30 min of reperfusion. Group II (Hyperthyroid IR group) were subjected to the same protocol of ischemia reperfusion. Group III (Hyperthyroid IR-OCT group): Hyperthyroid rats were supplemented with the somatostatin analogue, octreotide (OCT), 35 µg/kg subcutaneously, 20 minutes before sacrifice, followed by in-vitro study of cardiac responses to ischemia reperfusion. Blood samples were collected for measurement of plasma free T3, T4 and TSH. Coronary efflux lactate dehydrogenase levels were measured. Also, cardiac tissue malondialdehyde (MDA) levels and tumor necrosis factor alpha (TNF-α) levels were estimated. Results: Hyperthyroid (IR) rats revealed significant elevation in plasma free T3 and T4 with concomitant decrease in TSH levels. A significant reduction in final BW and BW gain were observed with higher absolute weights of left ventricle (LV) and cardiac index compared to the euthyroid controls. Systolic blood pressure (SBP) and mean arterial pressure (MAP) significantly elevated in non-treated hyperthyroid rats with a significant increase in their baseline chronotropic and inotropic activity compared to euthyroid control rats. But after ischemia those rats exhibited significantly higher degree of bradycardia (∆HR) and % change in heart rate (HR) compared to control rats. Moreover, significantly deteriorated post-ischemic recovery of inotropic parameters and significantly higher ∆ changes of these parameters were observed compared to euthyroid controls. These changes were accompanied by significant elevation in coronary efflux LDH levels and both cardiac tissue MDA and TNFα. Meanwhile, octreotide administration to hyperthyroid rats showed improvement of their baseline chronotropic and inotropic parameters as evidenced by the significantly reduced degree of bradycardia as well as significantly lower ∆ change of PT and PT/LV parameters compared to non-treated hyperthyroid rats. Such findings could be ascribed partly to the reduction of oxidative and inflammatory responses to IR as determined by the significantly decreased cardiac tissue MDA and TNFα respectively. Conclusion: Hyperthyroid hearts are less tolerant to ischemia/reperfusion injury with higher susceptibility to oxidative stress as well as overproduction of pro-inflammatory mediators. Thus, pharmacological targets that defend oxidative challenge and confer anti-inflammatory properties, namely octreotide (somatotstatin analogue) are considered to have potential therapeutic effect and may protect against myocardial ischemic damage in hyperthyroidism.

Integrative model of coronary flow in anatomically based vasculature under myogenic, shear, and metabolic regulation.

Coronary blood flow is regulated to match the oxygen demand of myocytes in the heart wall. Flow regulation is essential to meet the wide range of cardiac workload. The blood flows through a complex coronary vasculature of elastic vessels having nonlinear wall properties, under transmural heterogeneous myocardial extravascular loading. To date, there is no fully integrative flow analysis that incorporates global and local passive and flow control determinants. Here, we provide an integrative model of coronary flow regulation that considers the realistic asymmetric morphology of the coronary network, the dynamic myocardial loading on the vessels embedded in it, and the combined effects of local myogenic effect, local shear regulation, and conducted metabolic control driven by venous O2 saturation level. The model predicts autoregulation (approximately constant flow over a wide range of coronary perfusion pressures), reduced heterogeneity of regulated flow, and presence of flow reserve, in agreement with experimental observations. Furthermore, the model shows that the metabolic and myogenic regulations play a primary role, whereas shear has a secondary one. Regulation was found to have a significant effect on the flow except under extreme (high and low) inlet pressures and metabolic demand. Novel outcomes of the model are that cyclic myocardial loading on coronary vessels enhances the coronary flow reserve except under low inlet perfusion pressure, increases the pressure range of effective autoregulation, and reduces the network flow in the absence of metabolic regulation. Collectively, these findings demonstrate the utility of the present biophysical model, which can be used to unravel the underlying mechanisms of coronary physiopathology.

Sudden cardiac death owing to arrhythmogenic right ventricular cardiomyopathy

Background and objective:Arrhythmogenic right ventricular cardiomyopathy (ARVC) is increasingly recognized in forensic practice with controversial diagnosis. Here we described the epidemiological characteristics and reported the pathogenetic mechanism, diagnostic challenges, and forensic implications of Chinese ARVC autopsy cases.Methods:Two cases of sudden cardiac death owing to ARVC were reported. Retrospective analysis were performed on such 2 cases and 45 cases of separate ARVC complete autopsy case reports through Chinese literature databases in the last 30 years.Results:There were 27 males and 20 females, and the mean age at death was 35 years. Sudden cardiac death was the first manifestation observed in most patients, with no previous family and medical history. Exercise, acute stress, increased cardiac workload, and ethanol are frequently involved. The mean heart weight was 393 g (range, 240–590 g), and 10 cases had relative heart hypertrophy. Microscopic abnormalities included replacement of myocardium by adipose infiltration in 68.09% cases and fibroadipose in 31.91% cases; 80.85% cases were restricted to the right ventricle (RV), whereas biventricular subtype was seen in the remaining 19.15% cases. The preliminary quantitative histology showed 60.7% of fat tissues, 12.1% of fibrosis, and 27.2% residual myocytes in RV. Inflammatory cell infiltration was found in 25.53% cases, but myocyte necrosis was found in only 1 case. In 10.64% of cases, cardiac conduction was infiltrated by fibrosis, adipose, or both.Conclusion:In this review, the most characteristic and distinct histopathologic features that are diagnostic or highly suggestive of ARVC for forensic pathologists were identified. Combining gross and histological examinations with postmortem genetic analysis is recommended for identifying ARVC.

Preserved Cardiac Blood Supply-Workload Balance in Pediatric Patients After Aortic Arch Repair.

One of the most important problems in patients with aortic coarctation after aortic arch repair is future cardiovascular disease. We have previously reported that the enhancement of aortic pressure wave reflection in patients could be one of the causes of future cardiovascular diseases, because it results in an increase of the left ventricular workload and is disadvantageous for coronary circulation. Seventeen patients who had undergone aortic arch repair without pressure gradient in their aortic arch were enrolled. An ascending aortic pressure waveform was recorded by a pressure-sensor-mounted catheter, and a subendocardial viability ratio, which measures cardiac blood supply-workload balance, was calculated. The values were compared with those in age-matched controls. The patients' mean age was 6.8±2.8years. The mean ascending aortic systolic pressure was higher (100.4±12.9 vs. 90.2±8.9mmHg, p=0.0011) and the pulse pressure was wider (38.1±7.1 vs. 32.5±5.4mmHg, p=0.0072) in patients than in control subjects. There was no difference in the mean subendocardial viability ratio (1.01±0.25 vs. 1.01±0.24, ns), while the mean tension time index (27.4±5.6 vs. 23.0±3.3, p=0.0001) and diastolic pressure time index (28.4±11.1 vs. 23.6±8.0, p=0.0082) were higher in patients than in controls. The cardiac blood supply-workload balance was preserved in patients after aortic arch repair, despite an increase in their cardiac workload.

Surgical strategy for aortic arch reconstruction after the Norwood procedure based on numerical flow analysis.

Inefficient aortic flow after the Norwood procedure is known to lead to the deterioration of ventricular function due to an increased cardiac workload. To prevent the progression of aortic arch obstruction, arch reconstruction concomitant with second-stage surgery is recommended. The aim of this study was to determine the indications for reconstruction based on numerical simulation and to reveal the morphology that affects the haemodynamic parameters. Fifteen patients who underwent the Norwood procedure or arch repair and Damus-Kaye-Stansel anastomosis were enrolled. The pressure gradient in aortic arch was 1.6 ± 3.9 mmHg (ranged from 0 to 12 mmHg) on catheter examination. Six patients who had prominent turbulent flow accompanied with a large flow energy loss index greater than 40 mW/m2 and high wall shear stress greater than 100 Pa underwent arch reconstruction. After arch reconstruction, the energy loss index significantly decreased from 88.5 ± 50.0 mW/m2 to 23.1 ± 10.4 mW/m2 (P = 0.026) and wall shear stress significantly decreased from 194.5 ± 87.4 Pa to 60.3 ± 40.5 Pa (P = 0.0062). There were 3 late deaths due to heart failure caused by progressive atrioventricular valve regurgitation during the follow-up period (60 months). The systemic ventricular function was preserved in the remaining patients without any pressure gradients in the arch. Determining the surgical strategy for arch reconstruction based on numerical flow analysis may effectively reduce the ventricular load even if no stenosis or pressure gradients are observed on catheter examination or echocardiography.

Water ingestion decreases cardiac workload time-dependent in healthy adults with no effect of gender

Ingestion of water entails a variety of cardiovascular responses. However, the precise effect remains elusive. We aimed to determine in healthy adults the effect of water on cardiac workload and to investigate potential gender differences. We pooled data from two controlled studies where blood pressure (BP) and heart rate (HR) were continuously recorded before and after the ingestion of 355 mL of tap water. Additionally, we calculated double product by multiplying systolic BP with HR and evaluated spectral parameters referring to vagal tone. All parameters were investigated for potential differences based on gender. In response to water, HR, systolic BP, and double product decreased significantly during the first 30 min. However, these effects were attenuated for HR and double product and even abolished for systolic BP over the subsequent 30 min. Over the entire post-drink period (60 min), decreases in HR and double product (all P < 0.05) were observed. Spectral markers for vagal tone increased with the on-set of the water drink and remained elevated until the end (P < 0.005). No significant gender difference in cardiac workload parameters was observed. We provide evidence that drinking water decreases, in a time-dependent fashion, cardiac workload and that these responses appear not to be influenced by gender.

Cardiovascular mechanics in the early stages of pulmonary hypertension: a computational study.

We formulate and study a new mathematical model of pulmonary hypertension. Based on principles of fluid and elastic dynamics, we introduce a model that quantifies the stiffening of pulmonary vasculature (arteries and arterioles) to reproduce the hemodynamics of the pulmonary system, including physiologically consistent dependence between compliance and resistance. This pulmonary model is embedded in a closed-loop network of the major vessels in the body, approximated as one-dimensional elastic tubes, and zero-dimensional models for the heart and other organs. Increasingly severe pulmonary hypertension is modeled in the context of two extreme scenarios: (1) no cardiac compensation and (2) compensation to achieve constant cardiac output. Simulations from the computational model are used to estimate cardiac workload, as well as pressure and flow traces at several locations. We also quantify the sensitivity of several diagnostic indicators to the progression of pulmonary arterial stiffening. Simulation results indicate that pulmonary pulse pressure, pulmonary vascular compliance, pulmonary RC time, luminal distensibility of the pulmonary artery, and pulmonary vascular impedance are much better suited to detect the early stages of pulmonary hypertension than mean pulmonary arterial pressure and pulmonary vascular resistance, which are conventionally employed as diagnostic indicators for this disease.

ICD (Integrated Cardiac Device) Care through PACED (Patient-centred And Cardiac Nursing Engaged Device) Services in a Regional Hospital in Hong Kong

Introduction: Cardiac implantable electronic devices (CIED) are effective treatment to patients with bradycardia and life-threatening arrhythmia. However, without appropriate CIED settings and adaptation to life, patient may restrict activities for years. Furthermore, population of newly-implanted CIED patient has doubled in last decade. It challenged our service greatly, since cardiologist needs to follow up CIED patient *indefinitely in HK*. United Christian Hospital is a regional hospital serving a million populations. PACED services and ICD care were established here to provide intensive care during patient most needed period; and seamless integrated care along patient’s journey. “We are retaining not only heart rhythm, but helping patient’s life being PACED again” - That’s our motto. Methodology (CIED Patient Journey): Pre-operative: Patient is interviewed by cardiac nurse and ambulatory care nurse for pre-operative counselling and risk assessment. Implantation: Day admission and early discharge are facilitated with prior assessment. Acute phase: Patient will attend cardiology nurse clinic 1-2 weeks post-discharged for wound care; counselling & empowerment on living with device are delivered to both patient and family/caregiver; CIED functions are monitored under electro-diagnostic unit nurse assist. Between home and clinic, community nurse will visit patient and report for abnormality detected. Early phase: Intensive follow-up by cardiologist and cardiac nurse intermittently in first year. CIED functions are optimized based on unique patient’s physiological needs, e.g. life style, exercise capacity and age, etc. Retaining PACE of life: After condition stabilized, self-care ability and knowledge will be reassessed and reinforced in nurse clinic. Patient and family will join an integrated workshop collaborated by physiotherapist (PT), occupation-therapist (OT), social worker of health resource centre and cardiac nurse to meet with peer patients; and to retain confidence to live with device. Long term care: Protocol-driven regular device check-up intermittent with cardiac clinic to make sure safely function of CIED. Results: Data in 2015 were collected and analyzed. 1) Clinical: 180 patients were managed in nurse clinic. No adverse effect is noticed. Complications are now managed earlier e.g. wound problem; unstable lead parameter, etc. 30% patients with over-avoidance in daily-activity have showed improvement, some even retained job. 3.75% cases referred to cardiologist for e.g. symptomatic arrhythmia for treatment; lead-repositioning. 2) Client: Care ability and knowledge of patient / caregiver have improved from 52.6% to 96.3% and sustained at 87.2% in two-month evaluation. Patient surveys have shown high overall satisfaction at 98%; and have self-rated at 92% in retaining confidence to live with device. 3) Service utilization: Length of hospital stay is shortened; ~150 bed days are saved per year with pre-operative service. Over 600 nurse clinic attendances, cardiac clinic workload in early phase are thus alleviated by ~50%. New case waiting time is shortened in a consequence. Multidisciplinary referrals (~2%) were made e.g. OT for hypertrophic scar; PT for frozen shoulder, etc. Conclusion: ICD care and PACED services have demonstrated seamless collaboration among multidisciplinary for better patient outcomes. Delivering CIED services with cardiac nurse engagement is one of the pioneers among HK, and has achieved Hospital Authority nurse clinic accreditation in 2013.

Mitochondrial flashes regulate ATP homeostasis in the heart

The maintenance of a constant ATP level ('set-point') is a vital homeostatic function shared by eukaryotic cells. In particular, mammalian myocardium exquisitely safeguards its ATP set-point despite 10-fold fluctuations in cardiac workload. However, the exact mechanisms underlying this regulation of ATP homeostasis remain elusive. Here we show mitochondrial flashes (mitoflashes), recently discovered dynamic activity of mitochondria, play an essential role for the auto-regulation of ATP set-point in the heart. Specifically, mitoflashes negatively regulate ATP production in isolated respiring mitochondria and, their activity waxes and wanes to counteract the ATP supply-demand imbalance caused by superfluous substrate and altered workload in cardiomyocytes. Moreover, manipulating mitoflash activity is sufficient to inversely shift the otherwise stable ATP set-point. Mechanistically, the Bcl-xL-regulated proton leakage through F1Fo-ATP synthase appears to mediate the coupling between mitoflash production and ATP set-point regulation. These findings indicate mitoflashes appear to constitute a digital auto-regulator for ATP homeostasis in the heart.

Pathophysiology of Takotsubo Syndrome

Originally described by Japanese authors in the 1990s, Takotsubo syndrome (TTS) generally presents as an acute myocardial infarction characterized by severe left ventricular dysfunction. TTS, however, differs from an acute coronary syndrome because patients have generally a normal coronary angiogram and left ventricular dysfunction, which extends beyond the territory subtended by a single coronary artery and recovers within days or weeks. The prognosis was initially thought to be benign, but subsequent studies have demonstrated that both short-term mortality and long-term mortality are higher than previously recognized. Indeed, mortality reported during the acute phase in hospitalized patients is ≈4% to 5%, a figure comparable to that of ST-segment-elevation myocardial infarction in the era of primary percutaneous coronary interventions. Despite extensive research, the cause and pathogenesis of TTS remain incompletely understood. The aim of the present review is to discuss the pathophysiology of TTS with particular emphasis on the role of the central and autonomic nervous systems. Different emotional or psychological stressors have been identified to precede the onset of TTS. The anatomic structures that mediate the stress response are found in both the central and autonomic nervous systems. Acute stressors induce brain activation, increasing bioavailability of cortisol and catecholamine. Both circulating epinephrine and norepinephrine released from adrenal medullary chromaffin cells and norepinephrine released locally from sympathetic nerve terminals are significantly increased in the acute phase of TTS. This catecholamine surge leads, through multiple mechanisms, that is, direct catecholamine toxicity, adrenoceptor-mediated damage, epicardial and microvascular coronary vasoconstriction and/or spasm, and increased cardiac workload, to myocardial damage, which has a functional counterpart of transient apical left ventricular ballooning. The relative preponderance among postmenopausal women suggests that estrogen deprivation may play a facilitating role, probably mediated by endothelial dysfunction. Despite the substantial improvement in our understanding of the pathophysiology of TTS, a number of knowledge gaps remain.

Diagnosing and managing mitral regurgitation.

Mitral regurgitation is the most prevalent valvular disorder in the United States. Patient presentation varies from asymptomatic to symptoms of severe heart failure. Primary care providers often are the first to detect mitral regurgitation as a result of careful auscultation. Medical management focuses on reducing cardiac workload, combating cardiac remodeling, and treating left ventricular failure. Surgical management is reserved for severe cases.

EMPA-REG OUTCOME: The Cardiologist's Point of View

Cardiologists could view empagliflozin as a cardiovascular drug that also has a beneficial effect on reducing hyperglycemia in patients with type 2 diabetes mellitus (T2DM). The effects of empagliflozin in lowering the risk of cardiovascular death and hospitalization for heart failure in T2DM patients with high cardiovascular risk during the recent Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients-Removing Excess Glucose (EMPA-REG OUTCOME) trial may be explained principally in terms of changes to cardiovascular physiology; namely, by the potential ability of empagliflozin to reduce cardiac workload and myocardial oxygen consumption by lowering blood pressure, improving aortic compliance, and improving ventricular arterial coupling. These concepts and hypotheses are discussed in this report.